Project Summary Autism spectrum disorders (ASD) are highly prevalent, lifelong conditions characterized by impairments in social communication and the presence of restrictive, repetitive behaviors. Identifying the earliest signs of ASD is a critical factor in promoting optimal long-term outcomes for those affected. The developmental origins of ASD, including symptom onset and progression, remain poorly understood. Current known symptom-based markers of ASD are based on deviations in social and communicative skills that typically emerge around the first birthday; however, the presence of overt impairments reflects the consequence of an altered trajectory of social development, rather than the causes and underlying mechanisms from which these impairments arose. This has motivated the search for biomarkers more proximal to the source of deficits, including aberrations in early emerging neural systems that scaffold social development. Prior biomarker research has primarily focused the search within a single developmental domain, but this approach has fallen short of identifying a reliable risk marker of ASD within the first 12 months. Instead, infants who develop ASD may exhibit impairment across several developmental domains, including diminished social attention in both visual and auditory domains and atypical brain organization in early infancy. Furthermore, infant sibling research has not previously leveraged existing knowledge about autism-susceptibility genes?such as CNTNAP2, a gene strongly involved in the development of frontal-striatal networks integral for social cognition and communication?to examine relations between genetic variation and ASD-related phenotypes. The current proposal builds upon these bodies of research to provide a comprehensive profile of ASD risk in early infancy. The proposed studies will employ eye-tracking, neuroimaging, and neurobehavioral genetics to investigate developmental antecedents of the social and restrictive behavioral symptoms associated with ASD across early emerging domains critical for social development. Specifically, the studies will evaluate developmental trajectories in visual attention to faces from 3- to 12-months (Aim 1), the neural correlates of native language processing at 1.5 months (Aim 2), and early functional brain connectivity within the Salience Network at 1.5 months (Aim 3). Individual differences within each of these domains may index an infant's capacity to attend to, and learn from, socially relevant information in their immediate environments. Aim 4 examines whether early deviations in visual social attention to faces, early native language processing (as indexed by fMRI), and altered functional brain connectivity are affected by CNTNAP2 genotype. Taken together, the multimodal approach in the proposed studies will enhance our ability to detect infants most vulnerable for atypical social development and further our understanding of the developmental pathogenesis of ASD.